Aim:To explore the effects of cariporide,a selective sodium-hydrogen antiporterinhibitor,on endothelial dysfunction induced by high glucose.Methods:Acetyl-choline (ACh)-induced endothelium-dependent relaxation (EDR),sodium nitro-prusside (SNP)-induced endothelium-independent relaxation and biochemical pa-rameters including malondialdehyde (MDA),superoxide dismutase (SOD),andnitric oxide (NO) were measured in rat isolated aorta.Results:A 6-h incubationof aortic rings with high glucose (44 mmol/L) resulted in a significant inhibitionof EDR,but had no effects on endothelium-independent relaxation.After the 6-hincubation of aortic rings in the co-presence of cariporide (0.01,0.1,and 1 μmol/L)with high glucose,cariporide prevented the inhibition of EDR caused by highglucose in concentration-dependent manners.Similarly,high glucose decreasedSOD activity and contents of NO,and increased MDA concentration in aortictissue.Cariporide (1 μmol/L) significantly resisted the decrease of NO contentand SOD activity,and elevation of MDA concentration caused by high glucose inaortic tissues.Mannitol (44 mmol/L) or cariporide (1 μmol/L) alone had no ef-fect on EDR,endothelium-independent relaxation and biochemical parameters.Conclusion:Cariporide significantly prevented endothelial dysfunction inducedby high glucose.The mechanisms of endothelial dysfunction induced by highglucose may involve the activation of sodium-hydrogen antiporter and the gen-eration of oxygen-free radicals,but it is not related to the change of osmolarity. Aim: To explore the effects of cariporide, a selective sodium-hydrogen antiporter inhibitor, on endothelial dysfunction induced by high glucose. Methods: Acetyl-choline (ACh) -induced endothelium-dependent relaxation (EDR), sodium nitro-prusside induced endothelium-independent relaxation and biochemical pa-rameters including malondialdehyde (MDA), superoxide dismutase (SOD), and nitric oxide (NO) were measured in rat isolated aorta. Results: A 6-h incubation of aortic rings with high glucose (44 mmol / L) resulted in a significant inhibition of EDR but had no effects on endothelium-independent relaxation. After the 6-hincubation of aortic rings in the co-presence of cariporide (0.01, 0.1, and 1 μmol / L) with high glucose, cariporide prevented the inhibition of EDR caused by high glucose in concentration-dependent manners. Similarly, high glucose decreased SOD activity and contents of NO, and increased MDA concentration in aortictissue. Carboride (1 μmol / L) significantly resisted the decrease of NO content and SOD activity, and elevation of MDA concentration caused by high glucose inaortic tissues. Mannitol (44 mmol / L) or cariporide (1 μmol / L) alone had no ef-fect on EDR, endothelium-independent relaxation and biochemical parameters. Cariporide significantly induced endothelial dysfunction induced by high glucose. These mechanisms of endothelial dysfunction induced by high glucose. May be the activation of sodium-hydrogen antiporter and the gen-eration of oxygen-free radicals, but it is not related to the change of osmolarity.